详细信息
基于JAK2/STAT3信号通路探讨红芪多糖对糖尿病胃轻瘫大鼠炎症反应的影响 被引量:1
Effect of hedysarum polybotrys polysacchcaide on inflammation of diabetic gastroparesis rats based on JAK2/STAT3 signaling pathway
文献类型:期刊文献
中文题名:基于JAK2/STAT3信号通路探讨红芪多糖对糖尿病胃轻瘫大鼠炎症反应的影响
英文题名:Effect of hedysarum polybotrys polysacchcaide on inflammation of diabetic gastroparesis rats based on JAK2/STAT3 signaling pathway
作者:朱小利[1,2];安惠[1,2];李荣科[1];张磊[1];魏昭晖[1];苗琳琳[1,2];万生芳[1]
第一作者:朱小利
机构:[1]甘肃中医药大学基础医学院,甘肃兰州730000;[2]甘肃省中医方药挖掘与创新转化重点实验室,甘肃兰州730000
第一机构:甘肃中医药大学基础医学院(敦煌医学研究所)
年份:2024
卷号:40
期号:5
起止页码:907
中文期刊名:中国药理学通报
外文期刊名:Chinese Pharmacological Bulletin
收录:CSTPCD;;Scopus;北大核心:【北大核心2023】;CSCD:【CSCD2023_2024】;
基金:国家自然科学基金资助项目(No 82060914)。
语种:中文
中文关键词:糖尿病胃轻瘫;红芪多糖;胃黏膜损伤;JAK2/STAT3信号通路;胃肠动力;炎症反应
外文关键词:diabetic gastroparesis;hedysarum polybotrys polysacchcaide;gastric mucosal injury;JAK2/STAT3 signaling pathway;gastrointestinal motility;inflammatory reaction
摘要:目的研究红芪多糖(hedysarum polybotrys polysacchcaide,HPS)对糖尿病胃轻瘫(diabetic gastroparesis,DGP)大鼠胃黏膜炎症反应的影响及可能作用机制。方法62只雄性Wistar大鼠随机分为Control组12只及造模组50只,除Control组外,其余大鼠采用小剂量多次腹腔注射链脲佐菌素(25 mg·kg^(-1),连续3 d)联合高糖高脂饲料不规则喂养复制DGP模型,将成模大鼠随机分为Model组(灌胃纯净水)、HPS低、中、高剂量组(50、100、200 mg·kg^(-1)·d^(-1))及Metformin组(90 mg·kg^(-1)·d^(-1))分别灌胃处理,Control组给予等体积纯净水灌胃,每日1次,连续8周。HE染色观察各大鼠胃黏膜病理形态;ELISA检测大鼠胃黏膜TNF-α、IL-6、GAS、MTL含量;RT-PCR检测胃黏膜JAK2、STAT3 mRNA表达;Western blot检测胃黏膜JAK2、STAT3蛋白及磷酸化水平。结果与Control组相比,Model组大鼠HE染色胃黏膜有大量炎性细胞浸润;TNF-α、IL-6含量明显增加(P<0.01),GAS、MTL含量明显减少(P<0.01);JAK2、STAT3 mRNA表达明显升高(P<0.05);p-JAK2、p-STAT3明显升高(P<0.01)。与Model组相比,各给药组大鼠胃黏膜炎性表现有所改善;TNF-α、IL-6含量明显减少,GAS、MTL含量明显增加;JAK2、STAT3 mRNA表达明显降低;p-JAK2、p-STAT3表达明显降低(P<0.05)。结论HPS可改善大鼠胃黏膜炎症反应,修复胃黏膜损伤,其机制可能与调控JAK2/STAT3信号通路有关。
Aim To investigate the effects of hedysarum polybotrys polysacchcaide(HPS)on gastric mucosal inflammation of diabetic gastroparesis(DGP)rats and its possible mechanism.Methods A total of 62 male Wistar rats were randomly divided into the control group(12)and the modeling group(50).Except for the control group,the remaining rats were given multiple intraperitoneal injections of streptozotocin(25 mg·kg^(-1) for three consecutive days)and irregular feeding of high-sugar and high-fat diet to replicate DGP model.The model rats were randomly divided into the model group(intragastatically purified water),low,medium and high dose HPS groups(50,100,200 mg·kg^(-1)·d^(-1))and the metformin group(90 mg·kg^(-1)·d^(-1)),respectively,and the control group was intragastrically treated with equal volume of purified water once a day for eight weeks.The pathological morphology of gastric mucosa was observed by HE staining;the contents of TNF-α,IL-6,GAS and MTL in gastric mucosa were detected by ELISA.The expression of JAK2 and STAT3mRNA in gastric mucosa was detected by RT-PCR.The levels of JAK2 and STAT3 proteins and their phosphorylation in gastric mucosa were detected by Western blot.Results Compared with the control group,the gastric mucosa of the model group showed a large number of inflammatory cells infiltrated by HE staining.The contents of TNF-αand IL-6 significantly increased(P<0.01),while the contents of GAS and MTL significantly decreased(P<0.01).The mRNA expressions of JAK2 and STAT3 significantly increased(P<0.05).p-JAK2and p-STAT3 significantly increased(P<0.01).Compared with the model group,gastric mucosal inflammation was improved in each administration group.The contents of TNF-αand IL-6 decreased significantly,while the contents of GAS and MTL increased significantly.The mRNA expressions of JAK2 and STAT3 were significantly reduced.The expressions of p-JAK2 and p-STAT3 significantly decreased(P<0.05).Conclusions HPS can improve gastric mucosal inflammation and repair gastric mucosal damage in rats,and its mechanism may be related to the regulation of JAK2/STAT3 signaling pathway.
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